Published online Aug 15, 2024. doi: 10.4239/wjd.v15.i8.1654
Revised: May 14, 2024
Accepted: June 12, 2024
Published online: August 15, 2024
Processing time: 135 Days and 19.4 Hours
In this editorial, we comment on the article by Zhang et al. Diabetes mellitus is a chronic disorder associated with several complications like cardiomyopathy, neuropathy, and retinopathy. Diabetes prevalence is increasing worldwide. Multiple diabetes medications are prescribed based on individual patients’ needs. However, the exact mechanisms by which many of these drugs exert their pro-tective effects remain unclear. Zhang et al elucidates molecular mechanisms undelaying cardioprotective effect of the dipeptidyl peptidase-IV inhibitor, teneligliptin. Briefly, teneligliptin alleviates the activation of NOD-like receptor protein 3 inflammasome, a multiprotein complex that plays a pivotal role in regulating the innate immune system and inflammatory signaling. Suppression of NOD-like receptor protein 3 inflammasome activity reduces the expression of cytokines, oxygen radicals and inflammation. These findings highlight teneli
Core Tip: Zhang et al provided evidence that teneligliptin mitigated diabetic cardiomyopathy. The authors also clarified the undelaying molecular mechanisms, showing that teneligliptin inhibits NADPH oxidase 4, NOD-like receptor protein 3 inflammasome and activates activated protein kinase to maintain myocyte homeostasis. Researchers are encouraged to implement similar studies on humans to delineate the precise mechanism by which teneligliptin influences activated protein kinase and NOD-like receptor protein 3 signaling.